From a mechanistic angle, we showed that HDAC7 was overexpressed in BCR-ABL1− pre-B-ALL cells compared to normal bone marrow samples, and CC1007 could reduce the binding of HDAC7 at the promoters of monocyte–macrophage-specific genes via inhibition of HDAC7 expression and HDAC7:MEF2C interaction. The gene discussed is BCR; the disease is acute lymphoblastic leukemia.